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Biomedical subjects

T Forslund

Publications and source records attributed to T Forslund.

At least 55 records · Page 3Linked to original sources
PubMed1983

Sustained antihypertensive effect of captopril combined with diuretics and beta-adrenergic blocking drugs in patients with resistant hypertension.

Ten patients with severe hypertension and unsatisfactory blood pressure control during combined therapy with beta-adrenergic blocking drugs, diuretics, and vasodilators were treated with gradually increasing doses of captopril. Vasodilators were discontinued 24 hours prior to captopril administration. Six patients had essential, two renal, and two renovascular hypertension. Mild renal impairment was observed in four patients. Captopril effectively decreased blood pressure for 3 hours in all patients after the first dose. The antihypertensive effect appeared to be triphasic and was sustained in all but one patient during 12 months of observation. Captopril doses of 25-75 mg t.i.d. were sufficient to achieve acceptable blood pressure control (RR less than or equal to 160/100 mmHg) when given in the above mentioned combination. Side-effects were few and tolerable and discontinuation of captopril was not required.

Adrenergic beta-Antagonists↗
PubMed1983

Effect of time and dose on angiotensin converting enzyme during captopril treatment in the rat.

The effect of treatment time and dose of captopril with regard to angiotensin converting enzyme (ACE) in serum, lungs and kidneys of the rat were studied. Normotensive Wistar rats were treated with a constant dose of captopril (0.2 mg/ml) during various time periods. In a second study rats were treated with different captopril doses (6.25 micrograms, 12.5 micrograms, 25 micrograms, 50 micrograms, and 200 micrograms/ml water) during three weeks. Serum ACE activity and pulmonary and kidney plasma membrane ACE concentrations were measured in both studies. Captopril treatment resulted in a rapid decrease of ACE in pulmonary and kidney plasma membranes and a simultaneously increase of serum ACE activity during the first day of treatment. This was followed by increased membrane concentrations of ACE in the lungs and return to normal ACE concentrations in membranes of kidneys, presumably due to increased ACE biosynthesis. Serum ACE activity continued to increase during the whole study. Serum ACE activity increased in a dose dependent manner during treatment with different captopril doses. Increased plasma membrane ACE concentrations were not observed in the rats treated with captopril at doses below 200 micrograms/ml water.

Animals↗
PubMed1983

Decrease of serum angiotensin converting enzyme activity after discontinuation of captopril treatment.

Serum ACE activity increased as expected about three-fold following six weeks of captopril (30 mg/kg/day) treatment in Wistar rats (n = 9). The effect on serum and lung ACE activity and concentration, respectively, was studied after captopril discontinuation. Serum ACE activity was measured at start and 3, 6, and 12 days after captopril withdrawal. The approximal half-life of serum ACE activity was 72 hours as judged from the decrease rate after stimulated ACE biosynthesis induced by captopril. No differences in lung plasma membranes and lung homogenate ACE concentrations between treated and untreated rats were observed 12 days after discontinuation of captopril treatment. Serum ACE activity remained unchanged in the control rats (n = 9). We conclude that induction of ACE biosynthesis in the rat is reversible after withdrawal of captopril.

Animals↗
PubMed1983

Ultrasonic scanning after percutaneous renal biopsy.

Renal ultrasonic scanning was performed before and after 57 consecutive kidney biopsies in order to assess the value of this method in the diagnosis of complications. One large and six small perirenal haematomas were found, corresponding to an incidence of 13%. This figure is considerably larger than the incidence found with conventional diagnostic methods, but smaller than with computed tomography. One hydronephrosis and a blood clot in the urinary bladder were also diagnosed. No clinically significant complications were missed. We recommend ultrasonography as the first diagnostic procedure when biopsy complications are suspected.

Adolescent↗
PubMed1983

The induction of angiotensin converting enzyme by its inhibitors.

The inhibitors of angiotensin converting enzyme (ACE), captopril and enalapril, were found to increase ACE concentration in cultured human endothelial cells from cord artery as measured with a novel ACE assay employing MK 351A, an inhibitor of ACE, and with immunofluorescense labeling using anti-human lung ACE antibody. Dexamethasone (10 nM) also increased ACE and potentiated the increase of cellular ACE caused by captopril. Similar effects of ACE inhibitors were seen in cultured human macrophages, particularly after prestimulation with E. coli lipopolysaccharide. In Wistar Kyoto rats, captopril caused a 3-fold increase of serum ACE, while dexamethasone (40 ug/day, 14 days) did not increase serum ACE. Combined treatment with captopril and dexamethasone caused a 5-fold increase of ACE in purified lung plasma membranes. ACE inhibitors induce increased ACE biosynthesis in endothelial cells, and in macrophages. The rise of cellular ACE with ACE inhibitors is potentiated by glucocorticoid.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Regulation of angiotensin converting enzyme.

Angiotensin converting enzyme (ACE;EC 3.4.15.1), or kininase II, was studied in serum, cultured endothelial cells from cord artery, in macrophages of humans, and in serum and purified plasma membranes of rats following treatment with inducers of ACE biosynthesis. ACE activity was measured in biological fluids with an enzyme kinetic method employing synthetic 1-hipp-1-his-l-leu tripeptide as a substrate, and with a new method using 125I-labelled specific inhibitor of ACE as a sensitive probe for ACE binding sites. The latter technique also proved suitable for the quantification of ACE in cells. Anti-human ACE antibody was employed for immunofluorescence studies in human cells. Dexamethasone treatment caused an increase in ACE in cultured human endothelial cells, macrophages and in rat pulmonary plasma membranes, but failed to increase serum ACE activity in rats. Captopril and enalapril treatment of hypertensive patients increased total serum ACE, the increase being evident after removal of the active drug from the serum by prolonged storage or chloramine T treatment (captopril) or by dialysis (enalapril). Captopril increased the ACE content of endothelial cells and macrophages. Macrophages appeared sensitive to captopril induction of ACE biosynthesis after pre-stimulation with Escherichia coli lipopolysaccharide. Dexamethasone treatment potentiated the known induction of ACE in rat pulmonary tissue. Thus ACE biosynthesis may be enhanced by three categories of treatment: (1) glucocorticoid; (2) macrophage activation; (3) ACE inhibitors. The precise mechanism of ACE induction and its possible biological relevance await further clarification.

Adult↗
PubMed1982

Induction of angiotensin-converting enzyme with the ACE inhibitory compound MK-421 in rat lung.

Having observed that treatment of rats with captopril led to an increased ACE activity in serum and ACE concentration in lungs, we treated female Wistar Kyoto rats for 7 days with the esterified ACE inhibitor, MK-421 (1.0 mg/kg body weight per day), administered by Alzet osmotic minipump. Serum ACE activity decreased by 67% during MK-421 treatment when measured in non-dialyzed serum samples. Removal of the drug by dialysis unmasked a 280% increase of serum ACE activity. ACE concentration of crude lung homogenate increased 134% in MK-421-treated rats and ACE concentration in purified pulmonary plasma membranes increased by 34%. The increase of serum and lung ACE in MK-421-treated rats was similar to that seen in rats treated with captopril, and was probably due to induction of ACE biosynthesis. The mechanisms of this induction are unknown.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Induction of angiotensin I-converting enzyme in rat lung with captopril: the effect of adrenalectomy.

In spontaneously hypertensive rats, treatment with captopril, 0.2 g/liter of drinking fluid for 12 to 24 weeks, caused a threefold increase in serum angiotensin I-converting enzyme activity. Angiotensin I-converting enzyme increased 25 to 120 percent in lung plasma membranes. The elution profile of angiotensin I-converting enzyme on DEAE cellulose and after gel filtration on Sepharose 4B was unchanged by captopril. The Km value value also remained unchanged. In Wistar rats subjected to bilateral adrenalectomy, treatment with the same dose of captopril for 3 days resulted in increased serum angiotensin I-converting enzyme activity in both sham-operated and adrenalectomized rats, but angiotensin I-converting enzyme concentration increased in lung plasma membranes from sham-operated rats and captopril-treated rats only. We conclude that captopril causes induction of angiotensin-converting enzyme biosynthesis in spontaneously hypertensive and Wistar rats. The change is a quantitative one. Intact adrenal glands may be important for the incorporation of angiotensin I-converting enzyme into lung membranes.

Adrenal Glands↗
PubMed1981

Dissociation of the effect of captopril on blood pressure and angiotensin converting enzyme in serum and lungs of spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) of the Okamoto-Aoki strain (n = 40) were treated with captopril (SQ 14,225; D-3-mercapto-2-methylpropanoyl-L-proline) orally, dose 0.2 mg/ml in drinking water. The treatment was initiated early and later during the course of developing hypertension. Continuously treated rats did not develop hypertension. Rats receiving captopril for 12 weeks remained normotensive, whereas withdrawal of the drug resulted in hypertension. Captopril treatment was effective in the rats with established hypertension and decreased the blood pressures to nearly normal values. Serum angiotensin converting enzyme (ACE) activity rose 3-fold in captopril treated rats. ACE in lung plasma membranes increased during captopril treatment, indicating that captopril induced biosynthesis of pulmonary ACE. No qualitative differences were found in the ACE from treated and not treated animals. The dissociation of the antihypertensive effect of captopril and of increased ACE activity in serum and lungs reduce the value of relating blood pressure effects of the drug to measured enzyme activity in the SHR.

Animals↗
PubMed1980

Induction of angiotensin I-converting enzyme rat lung with Captopril (SQ 14225).

Angiotensin I-converting enzyme (ACE, EC 2.4.15.1.) was measured in serum and in pulmonary plasma membranes of 40 spontaneously hypertensive rats (SHR, Okamoto Aoki strain), divided into 4 groups, and treated with SQ 14225 (Captopril), 0.2 mg . ml-1 in drinking water, for 0-24 weeks. Serum ACE activity increased 2.5-3 fold after 12-24 weeks of SQ 14225 treatment, paralleled by an increase of ACE concentration in purified pulmonary plasma membranes (25-52%), and in ACE concentration upon solubilization with Triton X-100 from such plasma membranes (96-120%). We conclude that the ACE inhibitor, SQ 14225, causes marked induction of pulmonary ACE biosynthesis. High serum ACE activity probably reflects increased total biosynthesis of the enzyme.

Animals↗
PubMed1980

Kidney transplantation and tumours.

During the period 1964--1978 700 renal transplants were given to 602 patients. Eight patients had a history of tumour before transplantation. After transplantation six cases with a de novo tumour were found. The treatment of the pretransplant tumours was completed on average 3 years before transplantation. The average interval from transplantation to discovery of de novo tumour was 2 years. The pretransplant tumours appeared 5 to 9 years before last control (Jan. 79) (mean 8 years). Two of the transplanted patients with previous tumours died later of their tumours. The others are still alive. Two of the patients with de novo tumour died of vascular accidents and one of tumour. The other three are alive. It seems that transplantation can be successful in patients with previous tumours. This study does not support previous reports of increased risk of de novo tumours in transplanted patients.

Adolescent↗
PubMedDate not supplied

Renal transplant artery stenosis and percutaneous transluminal angioplasty.

Ten patients with renal transplant artery stenosis were treated with percutaneous transluminal angioplasty (PTA). All patients suffered from hypertension refractory to drug treatment. PTA was successful in five patients. Blood pressure improved significantly and the antihypertensive medication could be reduced or withdrawn. Acute angulation at the anastomosis prevented successful PTA in four patients. One inaccessible stenosis was corrected surgically. No significant complications arose. If a renal transplant artery stenosis is haemodynamically significant, PTA should be considered the method of first choice for correction.

Adult↗
PubMedDate not supplied

Peripheral blood lymphocyte subsets in radiologists exposed to ionizing radiation.

To investigate whether low dose ionizing radiation caused perturbation of peripheral blood lymphocytes in radiology unit staff, the T-helper/suppressor ratio was examined in eight radiologists exposed to low dose radiation over a period of 6 to 27 years (mean 12 years). No significant difference was noted in the T-cell subsets between exposed radiologists and non-exposed control subjects. The effect of low dose ionizing radiation on peripheral blood lymphocyte subsets seems to be virtually negligible. Further, measurement of the T-helper/suppressor ratio is not a reliable way of demonstrating any damage to bone marrow caused by low dose ionizing radiation.

Adult↗